Knockout of cytochrome P450 1A1 enhances lipopolysaccharide-induced acute lung injury in mice by targeting NF-κB activation.

Abstract:

:Acute lung injury (ALI) is accompanied by overactivation of multiple pro-inflammatory factors. Cytochrome P450 1A1 (CYP1A1) has been shown to aggravate lung injury in response to hyperoxia. However, the relationship between CYP1A1 and lipopolysaccharide (LPS)-induced ALI is unknown. In this study, CYP1A1 was shown to be upregulated in mouse lung in response to LPS. Using CYP1A1-deficient (CYP1A1-/-) mice, we found that CYP1A1 knockout enhanced LPS-induced ALI, as evidenced by increased TNF-α, IL-1β, IL-6, and nitric oxide in lung; these effects were mediated by overactivation of NF-κB and iNOS. Furthermore, we found that aspartate aminotransferase, lactate dehydrogenase, creatine kinase, and creatinine levels were elevated in serum of LPS-induced CYP1A1-/- mice. Altogether, these data provide novel insights into the involvement of CYP1A1 in LPS-induced lung injury.

journal_name

FEBS Open Bio

journal_title

FEBS open bio

authors

Tian LX,Tang X,Ma W,Wang J,Zhang W,Liu K,Chen T,Zhu JY,Liang HP

doi

10.1002/2211-5463.12977

subject

Has Abstract

pub_date

2020-09-15 00:00:00

issn

2211-5463

pub_type

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